Hepatocellular carcinoma, the third leading cause of cancer-related deaths globally, presents a critical public health burden in China due to its high incidence and mortality. While targeted therapies and immunotherapies have improved survival in advanced HCC, drug resistance remains a major therapeutic challenge. Recent studies suggest that gefitinib, an EGFR inhibitor, overcomes lenvatinib resistance, yet its mechanistic underpinnings are incompletely understood. To investigate gefitinib's metabolic effects in HCC, we conducted untargeted metabolomic profiling using two separate platforms: gas chromatography-mass spectrometry (GC-MS) and liquid chromatography-mass spectrometry (LC-MS) with both hydrophilic interaction liquid chromatography (HILIC) and reversed-phase modes. Raw data were processed by Mass Hunter, normalized with internal standards, and analyzed via SIMCA for pattern recognition. Principal component analysis (PCA) of quality control samples and experimental groups (n = 6 each) confirmed system stability and clear inter-group separation. Orthogonal projections to latent structures discriminant analysis models were validated by 200 permutation tests. Analysis identified 42 metabolites with VIP > 1, of which 25 showed significant alterations (p < 0.05) post-gefitinib treatment. KEGG/RaMP-DB enrichment revealed perturbations in four key pathways: arginine-proline metabolism, nitrogen metabolism, branched-chain amino acid biosynthesis, and taurine metabolism. These results delineate gefitinib-induced metabolic reprogramming in HCC cells, providing a foundation for targeting metabolic vulnerabilities to overcome therapy resistance.

The involvement of circular RNAs (circRNAs) have been well-documented in various cancers, including hepatocellular carcinoma (HCC); however, their regulatory roles in HIF-1α-mediated tumorigenesis remain largely unclear. This study elucidates the functional significance of N6-methyladenosine (m6A)-modified circRNA—circIST1 in HCC progression. Elevated expression of circIST1 was observed in both HCC clinical specimens and cultured cell lines. This pronounced upregulation was found to be associated with poor prognosis and survival. Functionally, circIST1 drives HCC progression by enhancing tumor cell proliferation, migration, and invasion and by inhibiting apoptosis, as validated in vitro and in vivo. Mechanistically, it functions as a competitive endogenous RNA (ceRNA) that sponges miR-140-3p and miR-182, thereby relieving their repression on the common downstream oncogene, HIF-1α. Rescue experiments confirm that the tumor-suppressive effects of circIST1 silencing are reversed upon inhibition of these miRNAs or overexpression of HIF-1α. Notably, we show that circIST1 drives HIF-1α-mediated aerobic glycolysis—a metabolic hallmark of cancer—-by enhancing glucose uptake, lactate production, and glycolytic flux. Furthermore, we identify methyltransferase-like 3 (METTL3)-dependent m6A modification as a critical regulator of circIST1 stability. Collectively, our findings uncover a novel m6A-circIST1-miR-140-3p/miR-182-HIF-1α regulatory axis that underlies metabolic reprogramming in HCC, positioning circIST1 as a promising therapeutic target for HCC metabolic intervention.

INTRODUCTION:The α7 nicotinic acetylcholine receptor (α7nAChR), a transmitter-gated ion channel, is normally activated by the endogenous neurotransmitter acetylcholine (ACh). Its activation triggers a distinctive cholinergic anti-inflammatory pathway, leading to anti-inflammatory effects in the central nervous system (CNS). This unique pharmacological property has positioned α7nAChR as a promising therapeutic target for multiple CNS disorders. This review delineates α7nAChR's multifaceted roles in CNS pathophysiology, appraises current clinical trial progress of its modulators, and elucidates key challenges and future directions for the development of next-generation therapeutics targeting α7nAChR. METHODS:Studies demonstrate that activation of α7nAChR represents a promising therapeutic strategy for diverse CNS disorders, including neurodegenerative, cerebrovascular, and neurodevelopmental diseases. RESULTS:Studies demonstrate that activation of the α7nAChR is a promising therapeutic strategy for diverse CNS diseases, including neurodegenerative, cerebrovascular, and neurodevelopmental diseases. DISCUSSION:This review highlights the core therapeutic value of α7nAChR in CNS disorders while identifying bottlenecks in its research and development. On one hand, preclinical studies show that α7nAChR's anti-inflammatory and neuroprotective effects support its potential as a therapeutic target. On the other hand, clinical trial data-including limited efficacy and dose-limiting cardiovascular adverse effects-reveal a persistent translational gap from preclinical to clinical. CONCLUSION:Although α7nAChR agonists hold considerable therapeutic potential, substantial challenges remain in clinical translation. Major hurdles include: (1) the inherent complexity of the CNS microenvironment, which affects receptor pharmacology; (2) insufficient subtype selectivity, leading to off-target effects; and (3) a scarcity of clinically efficacious compounds. Addressing these limitations is crucial for the successful development of α7nAChR-targeted therapies.

DDB1- and CUL4-associated factor 7 (DCAF7) has recently been identified as a critical regulator of tumorigenesis and a potential modulator of ferroptosis. However, the precise function of DCAF7 in regulating the progression of hepatocellular carcinoma (HCC) ferroptosis remains elusive. In this study, we demonstrate that DCAF7 and the deubiquitinase USP2 are highly expressed in HCC. Genetic ablation of DCAF7 or pharmacological inhibition of USP2 sensitizes HCC to ferroptosis and inhibits HCC progression both in vitro and in vivo. Mechanistically, DCAF7 recruits USP2 to inhibit clockophagy (the selective autophagic degradation of core clock protein BMAL1 mediated through p62/SQSTM1) by reducing BMAL1 K63-linked polyubiquitination. Targeting either DCAF7 or USP2 triggers clockophagy-induced ferroptosis through the HIF1α-SLC7A11 axis in HCC cells. Collectively, our study establishes DCAF7 and USP2 as novel suppressors of clockophagy-induced ferroptosis and reveals the potential therapeutic targets for HCC treatment.

Tyrosine kinase inhibitors (TKIs) are such as sorafenib the first-line therapeutic drugs for patients with advanced hepatocellular carcinoma. However, patients with TKI-resistant advanced liver cancer are insensitive to TKI treatment, resulting in limited survival benefits. This paper comprehensively reviewed the mechanisms underlying TKI resistance in hepatocytes, investigating activation of tumor signaling pathways, epigenetic regulation, tumor microenvironment, and metabolic reprogramming. Based on resistance mechanisms, it also reviews preclinical and clinical studies of drug resistance strategies and summarizes targeted therapy combined with immunotherapy currently in investigational clinical trials. Understanding the interactions and clinical studies of these resistance mechanisms offers new hope for improving and prolonging patient survival.

BackgroundThe IMforte trial demonstrated that lurbinectedin combined with atezolizumab (LU-AT) as a first-line regimen offers clinical advantages over atezolizumab alone (AT) in patients with extensive-stage small-cell lung cancer (ES-SCLC). However, given the high costs of lurbinectedin and atezolizumab, the cost-effectiveness of LU-AT relative to AT remains uncertain. This study aims to assess the cost-effectiveness of LU-AT as a first-line treatment for ES-SCLC within the context of China’s and the United States’ healthcare system.MethodsA partitioned survival analysis (PartSA) model was employed to assess the cost-effectiveness of LU-AT as a first-line treatment for ES-SCLC. Clinical efficacy data were sourced from the IMforte trial. Drug costs were based on national tender prices, while other costs and utility values were derived from the literature. Outcomes included total costs, quality-adjusted life years (QALYs), and incremental cost-effectiveness ratios (ICERs). One-way sensitivity analysis and probabilistic sensitivity analysis were conducted to assess the robustness of the model.ResultsThe combination regimen of lurbinectedin plus atezolizumab yielded an additional 0.21 QALYs compared with atezolizumab monotherapy, leading to an ICER of $374,167.43 per QALY in China and $1,071,237.82 per QALY in the USA, both beyond the willing-to-pay threshold ($40,365.00/QALY in China and $150,000.00/QALY in the USA). The utility of progression-free survival (PFS), the cost of lurbinectedin, body surface area (BSA), and the cost of atezolizumab are the four most influential factors in both China and the United States. Across all sensitivity analyses, the outcomes generated by the models remained robust. At a willingness-to-pay threshold of $40,365 and $150,000 per QALY, the probability of LU-AT being cost-effective relative to AT was 0% in China and USA.ConclusionWithin the framework of China’s and the United States’ healthcare system, LU-AT is unlikely to represent a cost-effective first-line treatment for ES-SCLC.

Gastrointestinal cancer is one of the most prevalent malignant tumors worldwide. The treatment landscape of gastrointestinal cancer has entered a new era with the advent of immunotherapy, which activates the immune system to identify and eliminate tumor cells. Immunotherapy has demonstrated high efficacy and tolerable toxicity profiles compared to conventional therapies. Immune checkpoint inhibitors including PD-1, PD-L1, CTLA-4 and LAG-3 in combination with targeted therapy or chemotherapy have been approved for the treatment of gastrointestinal tumors with good clinical patient benefit. In recent years, a variety of novel immunotherapeutic approaches have emerged. For example, adoptive T-cell therapy, such as claudin18.2-targeted CAR-T has achieved an objective remission rate of 48.6% in patients with advanced gastric cancer and gastroesophageal junction cancer. Oncolytic viruses inhibits tumor growth in both tumor lysis and immune activation, and is currently showing its efficacy against gastrointestinal tumors in some clinical trials. In addition, cancer vaccines, with their unique high degree of precision, have improved the effectiveness of individualized therapy. Personalized neoantigen vaccines combined with other immunotherapeutic drugs or chemotherapy, have shown some efficacy and safety in gastrointestinal patients. In this review, we summarize these recent advances in immunotherapy for the treatment of gastrointestinal tumors. Additionally, the challenges and limitations linked to immunotherapy were explored. This review will expand our understanding of clinical studies on immunotherapy in gastrointestinal cancer and assist in individualizing patient treatment strategies, maximizing therapeutic benefits, and improving patient prognosis.

BackgroundOsteoarthritis is characterized by articular cartilage degradation, involving inflammation-mediated chondrocyte apoptosis and extracellular matrix destruction. Eucommia ulmoides and Achyranthes bidentata constitute a classic herbal pair for OA treatment, yet their combinatorial effects and molecular mechanisms remain unelucidated.MethodsThe EU-AB extract was prepared via aqueous decoction. An LPS-induced ATDC5 chondrocyte inflammatory model and an MIA-induced rat OA model were established. Therapeutic efficacy was evaluated using Lequesne scores, ELISA, Western blotting, and immunohistochemistry. Bioactive components were identified by HPLC-TOF/MS, while RNA-seq and molecular interaction analyses validated underlying mechanisms.ResultsThe EU-AB extract significantly suppressed the expression of matrix metalloproteinases (MMP-3/13) and inflammatory cytokines (NO, TNF-α, IL-6, IL-1β) in both ATDC5 cells and rat serum (P < 0.05). Concurrently, it reduced Lequesne scores and joint swelling in MIA-induced OA rats (P < 0.05) while ameliorating histopathological cartilage damage. Among 35 compounds identified by HPLC-TOF/MS, pinoresinol diglucoside (PIN) from EU and chikusetsusaponin Ⅳa (CHI) from AB demonstrated synergistic effects, downregulating pro-apoptotic proteins (Caspase-3/9, Bax) through activation of the PI3K-Akt pathway and promotion of Akt phosphorylation.ConclusionThe herbal pair aqueous extract suppresses osteoarthritis via the bioactive component group CHI-PIN, demonstrating synergistic anti-inflammatory effects in MIA rats, likely mediated by PI3K-Akt-regulated apoptosis.

Photodynamic therapy (PDT) is an emerging treatment for melanoma stimulating antitumor immune responses. However, oxygen consumption by PDT exacerbates hypoxia and immunosuppression in the tumor microenvironment. This issue could potentially be addressed by M1 macrophages with high hydrogen peroxide concentrations, which can be catalyzed to oxygen, thereby increasing oxygen level and enhancing intrinsic immune response of M1 macrophages and their ability to stimulate adaptive immunity. Herein, biocompatible photosensitizer-containing nanoparticles were designed by combining bovine serum albumin and manganese dioxide (BMB). These nanoparticles were internalized by M1 macrophages in vitro to form nanoengineered macrophages (BMB@M1). BMB@M1 demonstrated various ways to transfer nanoparticles in melanoma with high tumor site accumulation. Within the tumor microenvironment characterized by hydrogen peroxide and acidity, BMB underwent Mn2+ transformation and generated oxygen. The paramagnetic property of Mn2+ was used for magnetic resonance imaging, enabling visualization of the melanoma enrichment process of BMB@M1. Oxygen supplementation enhanced the therapeutic effect of PDT and stimulated the secretion of IL-12 and IFN-gamma by macrophages, synergistically promoting the infiltration of T cells and dendritic cells into the tumor. These findings showed that nanoengineered M1 macrophage could be used as a delivery system to enhance immune effects of PDT.

Tumor immunotherapy is a promising approach for addressing the limitations of conventional tumor treatments, such as chemotherapy and radiotherapy, which often have side effects and fail to prevent recurrence and metastasis. However, the effectiveness and sustainability of immune activation in tumor immunotherapy remain challenging. Tumor immunogenic cell death, characterized by the release of immunogenic substances, damage associated molecular patterns (DAMPs), and tumor associated antigens, from dying tumor cells (DTCs), offers a potential solution. By enhancing the immunogenicity of DTCs through the inclusion of more immunogenic antigens and stimulating factors, immunogenic cell death (ICD) based cancer vaccines can be developed as a powerful tool for immunotherapy. Integrating ICD nanoinducers into conventional treatments like chemotherapy, photodynamic therapy, photothermal therapy, sonodynamic therapy, and radiotherapy presents a novel strategy to enhance treatment efficacy and potentially improve patient outcomes. Preclinical research has identified numerous potential ICD inducers. However, effectively translating these findings into clinically relevant applications remains a critical challenge. This review aims to contribute to this endeavor by providing valuable insights into the in vitro preparation of ICD-based cancer vaccines. We explored established tools for ICD induction, followed by an exploration of personalized ICD induction strategies and vaccine designs. By sharing this knowledge, we hope to stimulate further development and advancement in the field of ICD-based cancer vaccines.

SMYD3 (SET and MYND domain-containing 3) is a histone lysine methyltransferase highly expressed in different types of cancer(s) and is a promising epigenetic target for developing novel antitumor therapeutics. No selective inhibitors for this protein have been developed for cancer treatment. Therefore, the current study describes developing and characterizing a novel small molecule ZYZ384 screened and synthesized based on SMYD3 structure. Virtual screening was initially used to identify a lead compound and followed up by modification to get the novel molecules. Several technologies were used to facilitate compound screening about these novel molecules' binding affinities and inhibition activities with SMYD3 protein; the antitumor activity has been assessed in vitro using various cancer cell lines. In addition, a tumor-bearing nude mice model was established, and the activity of the selected molecule was determined in vivo. Both RNA-seq and chip-seq were performed to explore the antitumor mechanism. This work identified a novel small molecule ZYZ384 targeting SMYD3 with antitumor activity and impaired hepatocellular carcinoma tumor growth by reducing H3K4 trimethylation of the Rac1 promoter triggering the tumor cell cycle arrest through the AKT pathway.

Rationale: The bark of Eucommia ulmoides and the roots of Achyranthes bidentata are commonly used in traditional Chinese medicine, and their pairing appears in many traditional Chinese medicine formulas as a recognized compatible unit. However, the changes and interactions of the main components of these two formulas when paired remain unclear, and there is currently no standard or method for their quality control and assessment of pharmacological effects. Methods: An optimized ultra-high-performance liquid chromatography triple-quadrupole mass spectrometry (UHPLC-MS/MS) method was established for the simultaneous identification of 10 components in E. ulmoides and A. bidentata using in vitro and in vivo models. Tributyltin methacrylate was the internal standard solution, and the blood samples were treated by an organic solvent precipitation method. Gradient elution was conducted on a C18 column at 25 8C with 0.1% formic acid water:acetonitrile as the mobile phase at a flow rate of 0.5 mL min-1. Dynamic multiple response monitoring was performed in negative-ion mode using an Agilent Jet Stream electrospray ionization ion source. Results: In negative-ion detection mode, eucommiol exhibited a good response, and the isomers ginsenoside Ro and achyranthoside C could also be well separated. The developed method accurately detected the five components with a low blood content. Compared to controls, the levels of ginsenoside Ro, chikusetsusaponin IVa, and achyranthoside C increased; the contents of geniposidic acid and pinoresinol diglucoside were unchanged; and the levels of eucommiol, geniposide, beta-ecdysterone, genipin, and achyranthoside D decreased in vitro. In vivo, the contents of geniposidic acid, geniposide, pinoresinol diglucoside, and beta-ecdysterone were reduced; the contents of eucommiol and ginsenoside Ro were unchanged; and those of achyranthoside D, chikusetsusaponin IVa, and achyranthoside C increased compared to the corresponding levels in the internal control. Conclusions: A method for the quality control of the E. ulmoides-A. bidentata drug pair was established for the first time and the main components in 10 drug pairs could be determined simultaneously in vitro and in vivo. These findings show that the E. ulmoides and A. bidentata drug pair cause a compositional change, providing new ideas for the development of this combination to improve clinical efficacy.

体外膜肺氧合(ECMO)和连续肾脏替代治疗(CRRT)是重症感染患者的救治手段之一,对抗菌药物的药代动力/药效学存在一定的影响.现临床药师参与1例行ECMO联合CRRT治疗的重症肺炎患者的诊疗过程,建议医师对患者进行药物浓度监测并协助医师分析ECMO和CRRT对治疗药物药代动力学的影响,调整用药方案.经治疗后患者双肺炎症好转出院.临床药师为行ECMO联合CRRT治疗的严重感染患者提供个体化药学监护,能够提高治疗效果.

目的 了解某医院药品不良反应的发生特点及规律,为临床安全合理用药提供参考依据.方法 收集医院2017 年 1 月-2021 年 12 月上报的药品不良反应报告,回顾性分析患者性别、年龄、给药途径、药品种类、累及系统/器官及转归情况.结果 (1)867 例药品不良反应报告中,药品不良反应发生最多的类型是已知一般 674 例(77.74%);(2)男性 528 例(60.90%),女性 339 例(39.10%),45～64 岁患者最多(506 例,58.36%);(3)药品不良反应涉及的给药途径中静脉滴注发生率最高(664 例,76.23%);(4)药品不良反应涉及的药品种类中造影剂最多(171 例,19.63%),抗肿瘤药物、肝胆治疗药物及抗菌药物分别为第 2 和第 3 位;(5)药品不良反应累及系统/器官以皮肤及皮下组织最多(407 例,38.61%);(6)多数患者经治疗后可痊愈(847 例,97.69%).结论 药品不良反应的发生可能与患者性别、年龄、给药途径、药品种类等多种因素相关,临床医务人员应重视药品不良反应监测和上报工作,以更好地保障安全、合理用药.

Melanoma, a highly aggressive skin tumor, exhibits notable features including heterogeneity, a high mutational load, and innate immune escape. Despite advancements in melanoma treatment, current immunotherapies fail to fully exploit the immune system's maximum potential. Activating immunogenic cell death (ICD) holds promise in enhancing tumor cell immunogenicity, stimulating immune amplification response, improving drug sensitivity, and eliminating tumors. Nanotechnology-enabled ICD has emerged as a compelling therapeutic strategy for augmenting cancer immunotherapy. Nanoparticles possess versatile attributes, such as prolonged blood circulation, stability, and tumor-targeting capabilities, rendering them ideal for drug delivery. In this review, we elucidate the mechanisms underlying ICD induction and associated therapeutic strategies. Additionally, we provide a concise overview of the immune stress response associated with ICD and explore the potential synergistic benefits of combining ICD induction methods with the utilization of nanocarriers.

骨关节炎是人体关节生理性退化的表现,其发病原因复杂,具有难以逆转的特征.一氧化氮是关节产生病理变化的关键标志物之一,在骨关节炎患者的血液、关节滑液中均可检测到该分子及其合酶.近年来中药作为新药开发的重要来源之一,已成为国内治疗骨关节炎的一种核心方法.中药可通过对一氧化氮及其合酶的影响进而起到保护软骨、减轻局部炎症的作用,从而达到预防或缓解骨关节炎的目的.本文概述了骨关节炎中一氧化氮及其合酶的作用,并从中药复方、有效化学成分两个方面综述中药通过干预一氧化氮分子抑制骨关节炎的研究进展,指出了一氧化氮及其合酶与骨关节炎病程中关键信号通路之间的关系,提示中药可以通过靶向一氧化氮治疗骨关节炎的新思路.

目的 构建乌金胶囊活性成分-作用靶点网络和蛋白相互作用网络,对靶点涉及的功能以及通路进行分析,探讨乌金胶囊抗肝细胞癌作用机制.方法 通过TCMSP数据库()获取乌金胶囊中延胡索、郁金、黄芪、山楂和通关藤的主要活性成分及其靶点,通过GenCards、OMIM、TTD、DRUGBANK数据库获取肝细胞癌疾病相关靶点.采用Cyto-scape构建活性成分-肝细胞癌靶点网络,并分析核心成分和靶点;利用String()平台进行蛋白质相互作用分析;采用Metascape平台对靶点进行GO及KEGG通路分析.结果 筛选得到乌金胶囊活性成分66个,作用于139个肝细胞癌靶点;核心活性成分有槲皮素、山柰酚、柚皮素和刺芒柄花素等,核心靶点包括TGS2、HSP90AA1和RXRA等;GO分析结果表明,乌金胶囊抗肝细胞癌的靶点主要涉及细胞对氮化合物的反应、蛋白质磷酸化的正向调节、细胞对有机环状化合物的反应、细胞对生长因子刺激的反应和细胞对化学应激的反应等生物过程.KEGG分析结果显示,乌金胶囊抗肝细胞癌作用的靶点主要涉及磷脂酰肌醇3激酶/蛋白激酶B 信号通路、丝裂原活化蛋白激酶信号通路和肿瘤坏死因子等信号通路.结论 乌金胶囊抗肝细胞癌作用具有多成分、多靶点与多通路的特点,其可能通过调节磷脂酰肌醇3激酶/蛋白激酶B、丝裂原活化蛋白激酶和肿瘤坏死因子等相关通路发挥作用.

黑色素瘤是最具侵袭性的皮肤恶性肿瘤,易发生早期转移和治疗后复发.治疗性肿瘤疫苗是新兴的免疫疗法,具有毒性低以及可抑制肿瘤转移的特点.目前已有多个针对黑色素瘤治疗性疫苗的研究,其中黑色素瘤治疗性树突状细胞(DC)疫苗引起了广泛关注.虽然肿瘤治疗性DC疫苗在黑色素瘤中的疗效已被多项研究证实,但该类疫苗存在免疫效应不足、单独使用疗效不佳等问题,仍具有较大的改进空间.本文对黑色素瘤的治疗性DC疫苗的研究现状进行了综述,并对肿瘤治疗性DC肿瘤的研究重点及优化策略进行展望.

Renal cell carcinoma (RCC) is known to be the most commonly diagnosed kidney cancer. Clear cell RCC (ccRCC) represents approximately 85 % of diagnosed RCC cases. Targeted therapeutics, such as multi-targeted tyrosine kinase inhibitors (TKI) and mTOR inhibitors, are widely used in ccRCC therapy. However, patients treated with mTOR and TKI inhibitors easily acquire drug resistance, making the therapy less effective. Here, we demonstrated that circPTEN inhibits the expression of its parental gene PTEN by reducing methylation of the PTEN promotor and inhibits GLUT1 expression by reducing m6A methylation of GLUT1, which suppresses ccRCC progression and resistance to mTOR inhibitors.

目的 探讨肝胆外科肿瘤患者发生利奈唑胺相关性血小板减少的危险因素,为患者临床安全用药提供依据.方法 选取本院 2017年 1月至 2021年 12月间应用利奈唑胺进行抗感染治疗的肿瘤患者,根据给予利奈唑胺后是否出现血小板减少,将患者分为血小板减少组和未发生组.比较两组患者一般资料与实验室指标,采用多因素logistic回归分析筛选发生利奈唑胺相关性血小板减少的危险因素.结果 研究共纳入 104例患者,其中接受外科手术患者 84例,未接受外科手术患者 20例.利奈唑胺相关性血小板减少发生率为 24.0%.两组患者性别、年龄、利奈唑胺使用时长、血小板计数、白细胞计数、谷丙转氨酶(ALT)、谷草转氨酶(AST)、总胆红素、肌酐、估算肾小球滤过率有显著性差异(P<0.05);logistic回归分析结果提示,年龄≥60岁(OR=7.093;P=0.017)、利奈唑胺使用时长≥12 d(OR=4.399;P=0.035)、基础血小板计数≤200×109/L(OR=8.470;P=0.004)、基础AST≥50 U/L(OR=15.465;P<0.001)、基础白细胞计数≥11×109/L(OR=11.436;P=0.001)是肿瘤患者发生利奈唑胺相关性血小板减少的危险因素.结论 给肝胆外科肿瘤患者应用利奈唑胺时,医师需关注患者是否发生血小板减少的不良反应,尤其是年老、长疗程、基础血小板低、基础肝功能差及基础白细胞计数高的患者.